Subject(s)
Anisakiasis , Esophageal Neoplasms , Anisakiasis/diagnosis , Endoscopy , Esophagus/diagnostic imaging , Humans , Narrow Band ImagingABSTRACT
Pulmonary emphysema is characterized by persistent inflammation and progressive alveolar destruction. The receptor for advanced glycation end-products (RAGE) is a multiligand cell surface receptor reported to be involved in the process of acute alveolar epithelial cell injury. However, studies that address the role of RAGE in pulmonary emphysema are inconclusive. We investigated the role of RAGE in the development of elastase-induced pulmonary inflammation and emphysema in mice. RAGE-sufficient (RAGE(+/+)) mice and RAGE-deficient (RAGE(-/-)) mice were treated with intratracheal elastase on Day 0. Airway inflammation, static lung compliance, lung histology, and the levels of neutrophil-related chemokine and proinflammatory cytokines in bronchoalveolar lavage fluid were determined on Days 4 and 21. Neutrophilia in bronchoalveolar lavage fluid, seen in elastase-treated RAGE(+/+) mice, was reduced in elastase-treated RAGE(-/-) mice on Day 4, and was associated with decreased levels of keratinocyte chemoattractant, macrophage inflammatory protein-2, and IL-1ß. Static lung compliance values and emphysematous changes in the lung tissue were decreased in RAGE(-/-) mice compared with RAGE(+/+) mice on Day 21 after elastase treatment. Experiments using irradiated, bone marrow-chimeric mice showed that the mice expressing RAGE on radioresistant structural cells, but not hematopoietic cells, developed elastase-induced neutrophilia and emphysematous change in the lung. In contrast, mice expressing RAGE on hematopoietic cells, but not radioresistant structural cells, showed reduced neutrophilia and emphysematous change in the lung. These data identify the importance of RAGE expressed on lung structural cells in the development of elastase-induced pulmonary inflammation and emphysema. Thus, RAGE represents a novel therapeutic target for preventing pulmonary emphysema.
Subject(s)
Alveolar Epithelial Cells/metabolism , Pulmonary Emphysema/metabolism , Receptor for Advanced Glycation End Products/metabolism , Animals , Chemokines/metabolism , Dendritic Cells/metabolism , Female , Lung/metabolism , Lung/pathology , Macrophages, Alveolar/metabolism , Mice, Inbred C57BL , Mice, Knockout , Pulmonary Emphysema/immunology , Receptor for Advanced Glycation End Products/geneticsABSTRACT
Trastuzumab, a humanized monoclonal antibody against human epidermal growth factor receptor 2 (HER2), has been proven to result in a survival benefit for the treatment of patients with HER2-positive advanced gastric cancer (AGC). However, data are lacking for the treatment of those with disseminated intravascular coagulation (DIC) and diffuse bone marrow carcinomatosis. A 77-year-old woman presented with back pain and fatigue since 2 months. Esophagogastroduodenoscopy showed a scirrhous lesion in the gastric corpus, which was biopsied and identified as signet-ring cell carcinoma with HER2 overexpression on immunohistochemistry. Laboratory testing, bone scintigraphy, and bone marrow biopsy were conducted, and she was diagnosed with HER2-positive AGC with DIC and diffuse bone marrow carcinomatosis. She underwent chemotherapy with the following regimen: oral administration of 80 mg/m2 S-1 for 2 weeks and 6 mg/kg trastuzumab infusion on day 6 every 3 weeks, which significantly improved the DIC. She was discharged from the hospital 73 days after admission and survived for 438 days after diagnosis. To the best of our knowledge, this is the first case report in which HER2-positive AGC complicated by DIC with diffuse bone marrow carcinomatosis was successfully treated with combined chemotherapy consisting of S-1 plus trastuzumab.
Subject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Bone Marrow Neoplasms/drug therapy , Bone Neoplasms/drug therapy , Carcinoma, Signet Ring Cell/drug therapy , Disseminated Intravascular Coagulation/etiology , Stomach Neoplasms/drug therapy , Aged , Anticoagulants/therapeutic use , Biopsy , Bone Marrow Neoplasms/secondary , Bone Neoplasms/secondary , Carcinoma, Signet Ring Cell/chemistry , Disseminated Intravascular Coagulation/drug therapy , Drug Combinations , Fatal Outcome , Female , Humans , Oxonic Acid/administration & dosage , Receptor, ErbB-2/analysis , Stomach Neoplasms/pathology , Tegafur/administration & dosage , Trastuzumab/administration & dosageABSTRACT
The incidence of overlapping bronchial asthma and chronic obstructive pulmonary disease has increased in recent years. Cysteinyl leukotrienes (CysLTs) play an important role in asthma, and the type 1 CysLT receptor (CysLT1R) is expressed by many inflammatory cells. We evaluated the effect of montelukast, a CysLT1R antagonist, on mouse models of asthma, porcine pancreatic elastase (PPE)-induced emphysema, and asthma combined with emphysema. Mice were sensitized with ovalbumin (OVA) on Days 0 and 14 and subsequently challenged with OVA on Days 28, 29, and 30. Pulmonary emphysema was induced by intratracheal instillation of PPE on Day 25. Mice were treated subcutaneously with montelukast or vehicle from Day 25 to Day 31. Airway hyperresponsiveness (AHR), static compliance; the number of inflammatory cells, the levels of cytokines, chemokines, LTs, and perforin in the bronchoalveolar lavage fluid, and the quantitative morphometry of lung sections were analyzed on Day 32. Treatment with montelukast significantly attenuated the AHR and eosinophilic airway inflammation in OVA-sensitized and OVA-challenged mice. Administration of montelukast significantly reduced the AHR, static compliance, and neutrophilic airway inflammation, while attenuating emphysematous lung changes, in PPE-treated mice. In PPE-treated mice subjected to allergen sensitization and challenges, montelukast significantly suppressed the AHR, static compliance, and eosinophilic and neutrophilic airway inflammation in addition to the development of experimentally induced emphysema in the lungs. Our data suggest that CysLT1R antagonists may be effective in ameliorating the consequences of PPE-induced lung damage and the changes that follow allergen sensitization and challenges.
Subject(s)
Acetates/pharmacology , Asthma/drug therapy , Cysteine/metabolism , Leukotriene Antagonists/pharmacology , Leukotrienes/metabolism , Pulmonary Emphysema/drug therapy , Quinolines/pharmacology , Receptors, Leukotriene/metabolism , Animals , Asthma/metabolism , Bronchoalveolar Lavage Fluid , Chemokines/metabolism , Cyclopropanes , Female , Lung/drug effects , Lung/metabolism , Mice , Mice, Inbred BALB C , Pneumonia/drug therapy , Pneumonia/metabolism , Pulmonary Emphysema/metabolism , Sulfides , Tumor Necrosis Factor-alpha/metabolismSubject(s)
Edema/therapy , Immunosuppression Therapy , Multiple Organ Failure/therapy , Plasma Exchange , Systemic Inflammatory Response Syndrome/therapy , Thrombocytopenia/therapy , Edema/pathology , Female , Fibrosis , Humans , Middle Aged , Multiple Organ Failure/pathology , Syndrome , Systemic Inflammatory Response Syndrome/pathology , Thrombocytopenia/pathologySubject(s)
Carcinoma, Hepatocellular/complications , Endoscopy, Digestive System , Fibrin Tissue Adhesive/therapeutic use , Gastrointestinal Hemorrhage/drug therapy , Gastrointestinal Hemorrhage/etiology , Liver Neoplasms/complications , Polyglycolic Acid/therapeutic use , Aged , Fatal Outcome , Gastrointestinal Hemorrhage/diagnostic imaging , Humans , Male , Tomography, X-Ray ComputedABSTRACT
BACKGROUND: Chronic asthma is often associated with neutrophilic infiltration in the airways. Neutrophils contain elastase, a potent secretagogue in the airways, nonetheless the role for neutrophil elastase as well as neutrophilic inflammation in allergen-induced airway responses is not well defined. In this study, we have investigated the impact of neutrophil elastase inhibition on the development of allergic airway inflammation and airway hyperresponsiveness (AHR) in previously sensitized and challenged mice. METHODS: BALB/c mice were sensitized and challenged (primary) with ovalbumin (OVA). Six weeks later, a single OVA aerosol (secondary challenge) was delivered and airway inflammation and airway responses were monitored 6 and 48 hrs later. An inhibitor of neutrophil elastase was administered prior to secondary challenge. RESULTS: Mice developed a two-phase airway inflammatory response after secondary allergen challenge, one neutrophilic at 6 hr and the other eosinophilic, at 48 hr. PAR-2 expression in the lung tissues was enhanced following secondary challenge, and that PAR-2 intracellular expression on peribronchial lymph node (PBLN) T cells was also increased following allergen challenge of sensitized mice. Inhibition of neutrophil elastase significantly attenuated AHR, goblet cell metaplasia, and inflammatory cell accumulation in the airways following secondary OVA challenge. Levels of IL-4, IL-5 and IL-13, and eotaxin in BAL fluid 6 hr after secondary allergen challenge were significantly suppressed by the treatment. At 48 hr, treatment with the neutrophil elastase inhibitor significantly reduced the levels of IL-13 and TGF-ß1 in the BAL fluid. In parallel, in vitro IL-13 production was significantly inhibited in spleen cells from sensitized mice. CONCLUSION: These data indicate that neutrophil elastase plays an important role in the development of allergic airway inflammation and hyperresponsiveness, and would suggest that the neutrophil elastase inhibitor reduced AHR to inhaled methacholine indicating the potential for its use as a modulator of the immune/inflammatory response in both the neutrophil- and eosinophil-dominant phases of the response to secondary allergen challenge.
Subject(s)
Allergens , Bronchial Hyperreactivity/drug therapy , Glycine/analogs & derivatives , Inflammation/drug therapy , Leukocyte Elastase/physiology , Proteinase Inhibitory Proteins, Secretory/pharmacology , Respiratory Hypersensitivity/drug therapy , Sulfonamides/therapeutic use , Animals , Bronchi/pathology , Bronchial Hyperreactivity/pathology , Bronchoalveolar Lavage Fluid , Cells, Cultured , Chemokines/metabolism , Cytokines/metabolism , Female , Flow Cytometry , Glycine/pharmacology , Glycine/therapeutic use , Immunohistochemistry , Inflammation/pathology , Intercellular Signaling Peptides and Proteins/metabolism , Leukocyte Elastase/antagonists & inhibitors , Leukocyte Elastase/immunology , Mice , Mice, Inbred BALB C , Neutrophil Infiltration/physiology , Ovalbumin/immunology , Receptor, PAR-2/biosynthesis , Receptor, PAR-2/immunology , Respiratory Hypersensitivity/pathology , Sulfonamides/pharmacologyABSTRACT
BACKGROUND: Pulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. Although IL-17A contributes to many chronic inflammatory diseases, it's role in the inflammatory response of elastase-induced emphysema remains unclear. METHODS: In a model of elastase-induced pulmonary emphysema we examined the response of IL-17A-deficient mice, monitoring airway inflammation, static compliance, lung histology and levels of neutrophil-related chemokine and pro-inflammatory cytokines in bronchoalveolar lavage (BAL) fluid. RESULTS: Wild-type mice developed emphysematous changes in the lung tissue on day 21 after elastase treatment, whereas emphysematous changes were decreased in IL-17A-deficient mice compared to wild-type mice. Neutrophilia in BAL fluid, seen in elastase-treated wild-type mice, was reduced in elastase-treated IL-17A-deficient mice on day 4, associated with decreased levels of KC, MIP-2 and IL-1 beta. Elastase-treated wild-type mice showed increased IL-17A levels as well as increased numbers of IL-17A+ CD4 T cells in the lung in the initial period following elastase treatment. CONCLUSIONS: These data identify the important contribution of IL-17A in the development of elastase-induced pulmonary inflammation and emphysema. Targeting IL-17A in emphysema may be a potential therapeutic strategy for delaying disease progression.
Subject(s)
Inflammation Mediators/metabolism , Interleukin-17/metabolism , Lung/immunology , Pneumonia/immunology , Pulmonary Emphysema/immunology , Animals , Bronchoalveolar Lavage Fluid/immunology , Chemokines/metabolism , Female , Interleukin-17/deficiency , Interleukin-17/genetics , Lung/pathology , Lung/physiopathology , Lung Compliance , Mice , Mice, Inbred C57BL , Mice, Knockout , Neutrophils/immunology , Pancreatic Elastase , Pneumonia/chemically induced , Pneumonia/genetics , Pneumonia/pathology , Pneumonia/physiopathology , Pneumonia/prevention & control , Pulmonary Emphysema/chemically induced , Pulmonary Emphysema/genetics , Pulmonary Emphysema/pathology , Pulmonary Emphysema/physiopathology , Pulmonary Emphysema/prevention & control , Th17 Cells/immunology , Time FactorsABSTRACT
BACKGROUND: The survival advantage achieved by existing anti-cancer agents as second-line therapy for relapsed non-small cell lung cancer (NSCLC) is modest and further improvement of treatment outcome is desired. Combination chemotherapy with irinotecan and amrubicin for advanced NSCLC has not been fully evaluated. METHODS: The primary endpoint of this phase II clinical trial was objective response. Patients with NSCLC who had been treated previously with one or two chemotherapy agents were enrolled. Irinotecan and amrubicin were both administered on Days 1 and 8 of a 21-day cycle, at doses of 100 mg/m(2) and 40 mg/m(2), respectively. RESULTS: Between 2004 and 2006, 31 patients received a total of 101 courses; the median number of courses administered was three (range, one to six). Objective response was obtained in nine of the 31 patients (29.0% response rate; 95% confidence interval (CI), 12.1-46.0%). With a median follow-up time of 43.9 months, median survival time and the median progression-free survival time were 14.2 and 4.0 months, respectively. Myelosuppression was the most frequently observed adverse event, with grade 3/4 neutropenia in 51% of patients. Febrile neutropenia developed after nine courses (9%) and resulted in one treatment-related death. Cardiac toxicity and diarrhea, possibly specific for both agents, were infrequent and manageable. CONCLUSION: Combination chemotherapy with irinotecan and amrubicin is effective in patients with NSCLC but showed moderate toxicities in second- or third-line settings.
Subject(s)
Adenocarcinoma/drug therapy , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Carcinoma, Non-Small-Cell Lung/drug therapy , Carcinoma, Squamous Cell/drug therapy , Lung Neoplasms/drug therapy , Neoplasm Recurrence, Local/drug therapy , Salvage Therapy , Adenocarcinoma/mortality , Adenocarcinoma/pathology , Adult , Age Factors , Aged , Anthracyclines/administration & dosage , Camptothecin/administration & dosage , Camptothecin/analogs & derivatives , Carcinoma, Non-Small-Cell Lung/mortality , Carcinoma, Non-Small-Cell Lung/pathology , Carcinoma, Squamous Cell/mortality , Carcinoma, Squamous Cell/pathology , Female , Humans , Irinotecan , Lung Neoplasms/mortality , Lung Neoplasms/pathology , Male , Middle Aged , Neoplasm Recurrence, Local/mortality , Neoplasm Recurrence, Local/pathology , Neoplasm Staging , Prognosis , Survival RateABSTRACT
We report the case of a 63-year-old man who underwent annual surveillance esophagogastroduodenoscopy, during which a small squamous cell carcinoma and a tiny yellowish granular lesion were found in the middle esophagus, slightly apart from each other. Magnifying endoscopy with narrow-band imaging of the yellowish granular lesion showed yellowish spots and blots scattered within an approximately 2-mm area. The larger spots appeared nodular and were overlaid with tortuous microvessels. Subsequently, both the lesions were excised en masse via endoscopic submucosal dissection, and the yellowish lesion was determined to be xanthoma. Histologically, an aggregated nest of foam cells surrounded by intrapapillary capillary vessels filled the intraepithelial papillae; the foam cells also extended inferiorly, below the rete ridges, and were sparsely distributed through the lamina propria mucosae. To our knowledge, the latter finding is the first to be described in literature, which leads us to postulate that the number of foam cells in the lamina propria mucosae may affect how thick and yellow a xanthoma appears on endoscopy. We believe that this case that presents a highly detailed comparison between endoscopic and histologic findings improves our understanding of the endoscopic appearance of esophageal xanthomas and may facilitate a precise diagnosis of this rare disease.
Subject(s)
Carcinoma, Squamous Cell , Esophageal Neoplasms , Xanthomatosis , Carcinoma, Squamous Cell/complications , Carcinoma, Squamous Cell/diagnostic imaging , Carcinoma, Squamous Cell/surgery , Endoscopy, Gastrointestinal , Esophageal Neoplasms/complications , Esophageal Neoplasms/diagnostic imaging , Esophageal Neoplasms/surgery , Esophagoscopy/methods , Humans , Male , Middle Aged , Narrow Band Imaging , Xanthomatosis/complications , Xanthomatosis/diagnostic imaging , Xanthomatosis/surgeryABSTRACT
Most of the studies investigating the effectiveness of blocking the leukotriene B4 (LTB4) receptor 1 (BLT1) have been performed in models of primary or acute allergen challenge. The role of the LTB4-BLT1 pathway in secondary challenge models, where airway hyperresponsiveness (AHR) and airway inflammation have been established, has not been defined. We investigated the effects of blocking BLT1 on early- and late-phase development of AHR and airway inflammation in previously sensitized and challenged mice. Female BALB/c mice were sensitized (Days 1 and 14) and challenged (primary, Days 28-30) with ovalbumin. On Day 72, mice were challenged (secondary) with a single OVA aerosol, and the early and late phases of AHR and inflammation were determined. Specific blockade of BLT1 was attained by oral administration of a BLT1 antagonist on Days 70 through 72. Administration of the antagonist inhibited the secondary ovalbumin challenge-induced alterations in airway responses during the late phase but not during the early phase, as demonstrated by decreases in AHR and in bronchoalveolar lavage neutrophilia and eosinophilia 6 and 48 hours after secondary challenge. The latter was associated with decreased levels of KC protein, macrophage inflammatory protein 2, and IL-17 in the airways. These data identify the importance of the LTB4-BLT1 pathway in the development of late-phase, allergen-induced airway responsiveness after secondary airway challenge in mice with established airway disease.
Subject(s)
Anti-Asthmatic Agents/pharmacology , Asthma/drug therapy , Bronchial Hyperreactivity/drug therapy , Leukotriene Antagonists/pharmacology , Lung/drug effects , Pneumonia/drug therapy , Receptors, Leukotriene B4/antagonists & inhibitors , Animals , Antibodies/blood , Asthma/immunology , Asthma/physiopathology , Bronchial Hyperreactivity/immunology , Bronchial Hyperreactivity/physiopathology , Bronchial Provocation Tests , Bronchoalveolar Lavage Fluid/immunology , Chemokine CXCL1/metabolism , Chemokine CXCL2/metabolism , Disease Models, Animal , Female , Inflammation Mediators/metabolism , Interleukin-17/metabolism , Lung/immunology , Lung/physiopathology , Mice , Mice, Inbred BALB C , Neutrophil Infiltration/drug effects , Ovalbumin , Pneumonia/immunology , Pneumonia/physiopathology , Pulmonary Eosinophilia/immunology , Pulmonary Eosinophilia/prevention & control , Receptors, Leukotriene B4/metabolism , Time FactorsABSTRACT
Chemokine receptor (CCR) 5 is expressed on dendritic cells, macrophages, CD8 cells, memory CD4 T cells, and stromal cells, and is frequently used as a marker of T helper type 1 cells. Interventions that abrogate CCR5 or interfere with its ligand binding have been shown to alter T helper type 2-induced inflammatory responses. The role of CCR5 on allergic airway responses is not defined. CCR5-deficient (CCR5(-/-)) and wild-type (CCR5(+/+)) mice were sensitized and challenged with ovalbumin (OVA) and allergic airway responses were monitored 48 hours after the last OVA challenge. Cytokine levels in lung cell culture supernatants were also assessed. CCR5(-/-) mice showed significantly lower airway hyperresponsiveness (AHR) and lower numbers of total cells, eosinophils, and lymphocytes in bronchoalveolar lavage (BAL) fluid compared with CCR5(+/+) mice after sensitization and challenge. The levels of IL-4 and IL-13 in BAL fluid of CCR5(-/-) mice were lower than in CCR5(+/+) mice. Decreased numbers of lung T cells were also detected in CCR5(-/-) mice after sensitization and challenge. Transfer of OVA-sensitized T cells from CCR5(+/+), but not transfer of CCR5(-/-) cells, into CCR5(-/-) mice restored AHR and numbers of eosinophils in BAL fluid after OVA challenge. Accordingly, the numbers of airway-infiltrating donor T cells were significantly higher in the recipients of CCR5(+/+) T cells. Taken together, these data suggest that CCR5 plays a pivotal role in allergen-induced AHR and airway inflammation, and that CCR5 expression on T cells is essential to the accumulation of these cells in the airways.
Subject(s)
Allergens/toxicity , Gene Expression Regulation/immunology , Lung/metabolism , Receptors, CCR5/biosynthesis , Respiratory Hypersensitivity/metabolism , Animals , Bronchoalveolar Lavage , CD8-Positive T-Lymphocytes/immunology , CD8-Positive T-Lymphocytes/metabolism , CD8-Positive T-Lymphocytes/pathology , Cells, Cultured , Eosinophils/immunology , Eosinophils/metabolism , Eosinophils/pathology , Gene Expression Regulation/drug effects , Interleukin-13/biosynthesis , Interleukin-13/genetics , Interleukin-13/immunology , Interleukin-4/biosynthesis , Interleukin-4/genetics , Interleukin-4/immunology , Lung/immunology , Lung/pathology , Mice , Mice, Knockout , Receptors, CCR5/genetics , Receptors, CCR5/immunology , Respiratory Hypersensitivity/chemically induced , Respiratory Hypersensitivity/immunology , Respiratory Hypersensitivity/pathology , Th1 Cells/immunology , Th1 Cells/metabolism , Th1 Cells/pathology , Th2 Cells/immunology , Th2 Cells/metabolism , Th2 Cells/pathology , Time FactorsABSTRACT
Churg-Strauss syndrome (CSS) is a granulomatous necrotizing vasculitis of unknown etiology associated with bronchial asthma. Despite affecting small to medium-sized vessels, necrosis of the digits due to vasculitis is extremely rare. We report a case of CSS with necrosis of the toe tips. A 37-year-old woman with asthma, who had been diagnosed with CSS 2 years ago, was admitted to our hospital with an exacerbation of CSS. The patient had a high grade fever and complained of abdominal pain and numbness of the lower extremities. Blood examination revealed marked eosinophilia. The fever pattern, abdominal pain and blood eosinophilia showed improvement by combination treatment with prednisolone and cyclophosphamide. However, the color of her right toe tips changed, and necrosis finally resulted despite antithrombotic therapy. Arteriography showed narrowing of the dorsalis pedis artery and of the more peripheral arteries of her right leg. Stump plasty with negative pressure dressing therapy for the toe tips, but not amputation, was done to preserve the leg function. While numbness of the extremities remained, no recurrence of necrosis was seen. Clinicians need to be aware that rare complications of CSS, including necrosis of the digits, can occur.
Subject(s)
Churg-Strauss Syndrome/complications , Toes/pathology , Adult , Churg-Strauss Syndrome/pathology , Female , Humans , Necrosis/etiologyABSTRACT
INTRODUCTION: S-1 is an oral fluoropyrimidine-based combination of tegafur, gimeracil, and oteracil potassium. Although the combination of S-1 with carboplatin is a first-line chemotherapy regimen for advanced non-small cell lung cancer (NSCLC), the efficacy and safety of the regimen in the elderly remain unknown. METHODS: The patient inclusion criteria were previously untreated advanced NSCLC, wild-type epidermal growth factor receptor, aged 70 years or more, and a performance status (PS) of 0-2. The patients received oral S-1 (40mg/m2, twice daily) for 2 weeks and carboplatin (area under the curve: 5) on day 1 every 4 weeks as induction treatment. After four induction cycles, S-1 alone (40mg/m2, twice daily) was administered for 2 weeks every 4 weeks as a maintenance therapy until disease progression. The primary endpoint was the overall response rate (ORR), which was expected to exceed 20%, and the secondary endpoints included the disease control rate (DCR), progression-free survival (PFS), overall survival (OS), and the toxicity profile. The associations between clinical outcomes and expression of genes such as thymidylate synthase and thymidine phosphorylase in the tumors were evaluated. RESULTS: Thirty-three patients were enrolled between March 2013 and June 2015. The median age was 78 (range 70-89) years, and 51.5% had a PS of 0. The ORR was 30.3% (95% confidence interval (CI): 14.6-46.0) and the DCR 57.6% (95% CI: 40.7-74.4). Grade 3/4 toxicities included thrombocytopenia (42.4%), neutropenia (33.3%), and anemia (27.3%). There was one treatment-related death due to aspiration pneumonia following febrile neutropenia. The median PFS and OS were 134days (95% CI: 79-173) and 479days (95% CI: 250-571), respectively. Low thymidine phosphorylase expression was associated with the DCR (P<0.01). CONCLUSION: This study met the predesigned primary endpoint, and the regimen seems to be a favorable treatment option.
Subject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Carcinoma, Non-Small-Cell Lung/drug therapy , Carcinoma, Non-Small-Cell Lung/pathology , Lung Neoplasms/drug therapy , Lung Neoplasms/pathology , Aged , Aged, 80 and over , Antineoplastic Combined Chemotherapy Protocols/adverse effects , Biomarkers, Tumor , Carboplatin/administration & dosage , Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/mortality , Drug Combinations , ErbB Receptors/genetics , Female , Gene Expression Profiling , Humans , Lung Neoplasms/genetics , Lung Neoplasms/mortality , Male , Neoplasm Staging , Oxonic Acid/administration & dosage , Survival Analysis , Tegafur/administration & dosage , Treatment OutcomeABSTRACT
Capsule endoscope aspiration into the respiratory tract is a rare complication of capsule endoscopy. Despite the potential seriousness of this complication, no accepted methods exist to accurately predict and therefore prevent it. We describe the case of an 85-year-old male who presented for evaluation of iron deficiency anemia. He complained of dysphagia while ingesting a patency capsule, with several attempts over a period of 5 min before he was successful. Five days later, he underwent capsule endoscopy, where he experienced similar symptoms in swallowing the capsule. The rest of the examination proceeded uneventfully. On reviewing the captured images, the capsule endoscope was revealed to be aspirated, remaining in the respiratory tract for approximately 220 s before images of the esophagus and stomach appeared. To our knowledge, this is the first documented case of a patient who experienced capsule endoscope aspiration after ingestion of a patency capsule. This case suggests that repeated attempts required for ingesting the patency capsule can predict capsule endoscope aspiration. We presume that paying sufficient attention to the symptoms of a patient who ingests a patency capsule could help us prevent serious complications such as aspiration of the capsule endoscope. In addition, this experience implies the potential risk for ingesting the patency capsule. We must be aware that the patency capsule could also be aspirated and there may be more unrecognized aspiration cases.